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Updated: Oct 27, 2025

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Published on: June 20, 2020
QTc interval prolongation, inflammation, and mortality in patients with COVID-19
Simone Gulletta1, Paolo Della Bella1, Luigi Pannone2
1Arrhythmia Unit and Electrophysiology Laboratories, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Purpose:
Systemic inflammation has been associated with corrected QT (QTc) interval prolongation. The role of inflammation on QTc prolongation in COVID-19 patients was investigated.
Methods:
Patients with a laboratory-confirmed SARS-CoV-2 infection admitted to IRCCS San Raffaele Scientific Institute (Milan, Italy) between March 14, 2020, and March 30, 2020 were included. QTc-I was defined as the QTc interval by Bazett formula in the first ECG performed during the hospitalization, before any new drug treatment; QTc-II was the QTc in the ECG performed after the initiation of hydroxychloroquine drug treatment.
Results:
QTc-I was long in 45 patients (45%) and normal in 55 patients (55%). Patients with long QTc-I were older and more frequently males. C-Reactive protein (CRP) and white blood cell (WBC) count at hospitalization were higher in patients with long QTc-I and long QTc-II. QTc-I was significantly correlated with CRP levels at hospitalization. After a median follow-up of 83 days, 14 patients (14%) died. There were no deaths attributed to ventricular arrhythmias. Patients with long QTc-I and long QTc-II had a shorter survival, compared with normal QTc-I and QTc-II patients, respectively. In Cox multivariate analysis, independent predictors of mortality were age (HR = 1.1, CI 95% 1.04-1.18, p = 0.002) and CRP at ECG II (HR 1.1, CI 95% 1.0-1.1, p = 0.02).
Conclusions:
QTc at hospitalization is a simple risk marker of mortality risk in COVID-19 patients and reflects the myocardial inflammatory status.
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